Pulmonary capillary permeability and pulmonary microangiopathy in diabetes mellitus

Krzemieniecki, Krzysztof; Pieńkowska, Joanna; Słomiński, W.; Jassem, Ewa; Studniarek, Michał

doi:10.1016/j.diabres.2015.02.033

Cited by 12 publications

(11 citation statements)

References 16 publications

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“…Impaired lung function is characterized by abnormal pulmonary vascular responsiveness, microvascular dysfunction, platelet activation, and lung fibrosis [8,25,26,27]. Microvascular injury is a well-known complication of diabetes that is likely to target multiple organs and contributes to the development of cardiac and pulmonary fibrosis.…”

Section: Diabetic Lung Fibrosismentioning

confidence: 99%

“…The concept of diabetes-induced pulmonary microvascular dysfunction is well recognized [17,27], but changes in the pulmonary microenvironment likely to cause pro-thrombotic responses via interactions between platelets, blood flow and the vascular endothelium have not been well characterized [37]. Platelets play a significant role in acute lung injury in initiating inflammation, increasing microvascular leakage, and promoting ventilation/perfusion mismatch [38,39,40].…”

Section: A Role For Platelets In the Pathology Of Diabetes-inducedmentioning

confidence: 99%

“…Diabetes detrimental systemic effect, with excessive NO combined with ROS, may directly contribute to platelet activation and cause chronic inflammation associated with damaged lung capillary endothelium and microangiopathy (Figure 3) [27,49,62,63]. Streptozotocin-induced diabetes caused pulmonary endothelial dysfunction in rats by enhancing NADPH oxidase-derived superoxide production, impairing dilation to acetylcholine and reducing vasoconstriction to inhibition of nitric oxide.…”

Section: Putative Signaling Mediating Diabetes-induced Microvasculmentioning

confidence: 99%

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Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Jagadapillai

Rane

Lin

et al. 2016

IJMS

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Diabetes is strongly associated with systemic inflammation and oxidative stress, but its effect on pulmonary vascular disease and lung function has often been disregarded. Several studies identified restrictive lung disease and fibrotic changes in diabetic patients and in animal models of diabetes. While microvascular dysfunction is a well-known complication of diabetes, the mechanisms leading to diabetes-induced lung injury have largely been disregarded. We described the potential involvement of diabetes-induced platelet-endothelial interactions in perpetuating vascular inflammation and oxidative injury leading to fibrotic changes in the lung. Changes in nitric oxide synthase (NOS) activation and decreased NO bioavailability in the diabetic lung increase platelet activation and vascular injury and may account for platelet hyperreactivity reported in diabetic patients. Additionally, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway has been reported to mediate pancreatic islet damage, and is implicated in the onset of diabetes, inflammation and vascular injury. Many growth factors and diabetes-induced agonists act via the JAK/STAT pathway. Other studies reported the contribution of the JAK/STAT pathway to the regulation of the pulmonary fibrotic process but the role of this pathway in the development of diabetic lung fibrosis has not been considered. These observations may open new therapeutic perspectives for modulating multiple pathways to mitigate diabetes onset or its pulmonary consequences.

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Section: Diabetic Lung Fibrosismentioning

confidence: 99%

Section: A Role For Platelets In the Pathology Of Diabetes-inducedmentioning

confidence: 99%

Section: Putative Signaling Mediating Diabetes-induced Microvasculmentioning

confidence: 99%

See 1 more Smart Citation

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Jagadapillai

Rane

Lin

et al. 2016

IJMS

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“…Included and excluded studies were collected following the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) flow diagram (Kahnert et al, 2017). This meta‐analysis was performed according to the Meta‐analysis Of Observational Studies in Epidemiology (MOOSE) guidelines (Kuziemski, Pienkowska, Slominski, Jassem, & Studniarek, 2015).…”

Section: Methodsmentioning

confidence: 99%

Obstructive sleep apnea is associated with coronary microvascular dysfunction: A systematic review from a clinical perspective

Zhang

Zhao

Shu

et al. 2020

Journal of Sleep Research

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Coronary microvascular dysfunction (CMD) is proposed to be a contributor to the signs and symptoms of myocardial ischaemia, which results from a limited microvascular vasodilator capacity under vasodilator stimuli (Crea, Camici, & Bairey Merz, 2014). Coronary flow reserve (CFR), quantified as the ratio of hyperaemic to rest myocardial blood flow, is a functional measure of large-and small-vessel ischaemia, and in the absence of overt coronary artery disease (CAD), is a marker of CMD (Taqueti et al.,

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“…Besides that, alterations in the structure and function of the complex pulmonary microcirculatory network have been observed, as well as a positive relationship between lung permeability and pulmonary microangiopathy in diabetic patients (Kuziemski et al , 2015). A few molecular mechanisms of pulmonary microvascular permeability during diabetes have been elucidated.…”

Section: Microvascular Hyperpermeability In Injury or Disease Conditionsmentioning

confidence: 99%

Endothelial Protrusions in Junctional Integrity and Barrier Function

Alves

Motawe

Yuan

et al. 2018

Current Topics in Membranes

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Endothelial cells of the microcirculation form a semi-permeable diffusion barrier between the blood and tissues. This permeability of the endothelium, particularly in the capillaries and postcapillary venules, is a normal physiological function needed for blood-tissue exchange in the microcirculation. During inflammation, microvascular permeability increases dramatically and can lead to tissue edema, which in turn can lead to dysfunction of tissues and organs. The molecular mechanisms that control the barrier function of endothelial cells have been under investigation for several decades, and remain an important topic due to the potential for discovery of novel therapeutic strategies to reduce edema. This review highlights current knowledge of the cellular and molecular mechanisms that lead to endothelial hyperpermeability during inflammatory conditions associated with injury and disease. This includes a discussion of recent findings demonstrating temporal protrusions by endothelial cells that may contribute to intercellular junction integrity between endothelial cells and affect the diffusion distance for solutes via the paracellular pathway.

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Pulmonary capillary permeability and pulmonary microangiopathy in diabetes mellitus

Cited by 12 publications

References 16 publications

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Diabetic Microvascular Disease and Pulmonary Fibrosis: The Contribution of Platelets and Systemic Inflammation

Obstructive sleep apnea is associated with coronary microvascular dysfunction: A systematic review from a clinical perspective

Endothelial Protrusions in Junctional Integrity and Barrier Function

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